Epidermis-intrinsic transcription factor Ovol1 coordinately regulates barrier maintenance and neutrophil accumulation in psoriasis-like inflammation

Skin epidermis constitutes the exterior barrier that protects the body from dehydration and environmental assaults. Barrier defects underlie common inflammatory skin diseases, but the molecular mechanisms that maintain barrier integrity and regulate epidermal-immune cell cross-talk in inflamed skin are not fully understood. Here we show that skin epithelia-specific deletion of Ovol1 (ovo-like 1), which encodes a skin disease-linked transcriptional repressor, impairs the epidermal barrier and aggravates psoriasis-like skin inflammation in mice in part through enhancing neutrophil accumulation and abscess formation.
Source: Journal of Investigative Dermatology - Category: Dermatology Authors: Tags: Original Article Source Type: research